It is desired that the present proposal be undetaken to delineate the cellular mechanisms causing myocardial dysfunction following burn injury, endotoxemia, and hemorrhage in hopes to clarify the role of the heart in the development of shock, particularly during the irreversible stage. The proposed experiments involve the following aspects: Identification of metabolic alterations in the uptake and utilization of free fatty acid, glucose and lactate by myocytes isolated from adult animals after burn injury and experimentally produced shock and elucidation of the mechanisms causing these alterations; assessment of the relative contribution to myocardial energy production of either fatty acid or carbohydrate substrate; identification of non-equilibrium reactions and regulatory enzymes in glycolytic and TCA cycle pathways; elucidation of the mechanisms regulating oxidation and esterification of long-chain fatty acid and determination of factors causing triglyceride accumulation in the heart; and analysis of the burn injured and shock-induced changes in myocardial lipid constituents and in the molecular structure of triglyceride and major sub-classes of phospholipids. The information to be obtained from these studies will be useful in understanding the basic mechanisms responsible for dysfunction of heart following the systemic insult mentioned above, and thus may contribute to the planning of treatment of burn and shock patients.